Patients with chronic alcoholism are predisposed to infections, and in particular, to pneumonia. Current concepts suggest that the recruitment of inflammatory cells (neutrophils) into the lower respiratory tract is important in host defense. The hypothesis of this grant application is that one mechanism which may account for the high incidence of pneumonia in alcoholics is the inability to adequately recruit inflammatory cells into the lung. To test this hypothesis patients with alcoholic hepatitis would undergo bronchoalveolar lavage and patients with nonalcoholic liver disease and normal volunteers would serve as control populations. The two principle mechanisms of recruitment would be examined using the material obtained from bronchoalveolar lavage: 1. Complement activation; and 2. Release of leukotriene B4 by the alveolar macrophage. The former mechanism would be assessed by determining the levels of the complement proteins Properdin factor B, C3, and C5 in the sera, bronchoalveolar lavage, and alveolar macrophage culture supernatants and comparing the results between the alcoholic patients and controls. The latter mechanism would be assessed by culturing alveolar macrophages and determining the ability of these cells to release chemotactic activity and leukotrine B4 into their culture supernatants when stimulated. An inhibitor of both complement-derived neutrophil chemotaxis and macrophage-derived neutrophil chemotaxis (chemotactic factor inactivator) exists in higher concentrations in the sera of patients with alcoholic hepatitis. The bronchoalveolar lavage fluid of these patients would be examined to determine if these elevated serum levels of chemotactic factor inactivator are reflected in the lower respiratory tract. These studies would determine if the release of inflammatory mediator is abnormal in the lower respiratory tract of alcoholics and may provide insights into determining the mechanisms accounting for the abnormal host defense seen in these patients.